Young Man with Very Fast Regular Wide Complex Tachycardia

EMS was dispatched for a 30-something male who feels his heart is racing.  Sudden onset.

The patient had no previous medical history.

Vitals were normal except for a heart rate of 226.

A prehospital 12-lead was recorded:

There is a regular wide complex tachycardia.  The computer diagnosed this as Ventricular Tachycardia.

Is it definitely VT??

The patient was given 6mg, then 12 mg, of adenosine, without a change in the rhythm.

He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded.

The bedside ultrasound (video not available) reportedly showed only a slightly reduced LV function.

Here is the ECG:

What do you think?

There is a wide complex regular tachycardia at a rate of 226.  The first part of the QRS is slow onset (see magnification below).  The differential is VT vs. AVRT.  

Could it be RVOT (Right ventricular outflow tract VT).  No, this requires inferior axis and LBBB morphology.  There is no inferior axis.

RVOT VT:

A 40-something without past history presents with wide complex tachycardia and crushing chest pain

 

Regular Wide Complex Tachycardia. What is the Diagnosis?

Toothache, incidental Wide Complex Tachycardia

Could it be fascicular VT or Bundle Branch VT (i.e., idiopathic VT)?   No, because the first part of the QRS is slow onset (see magnified V1-V6 below).

Could it be standard VT?  Yes, but this would be unusual in someone with no cardiac history and a reasonably good contractility on echo.

Could it be AVRT?  Yes.

If AVRT, adenosine is likely to work, but it did not work in the prehospital setting.  

Perhaps:

1) it is VT 

2) the dose of adenosine was too low or

3) the adenosine was not given fast enough.

V1-V6 magnified, with lines marking onset of QRS and end of first part of QRS:

From the onset of the QRS to the nadir of the S-wave is greater than 100 ms, which is not consistent with a SVT with aberrancy or with VT that is initiated in conducting fibers (idiopathic VT such as posterior fascicular VT or BBB VT).

Thus, this is more likely:

1) antidromic AVRT (down through accessoary pathway and up through the AV node OR

2) standard VT which begins in myocardium and thus has a wider initial part of the QRS.

Case continued.

The patient was immediately electrically cardioverted.

Here is the post cardioversion ECG:

What do you think?

The initial ECG could be either VT or Antidromic AV Reciprocating Tachycardia (using an accessary pathway -- in other words, WPW).

Does a post cardioversion ECG without delta waves rule out WPW?

No.  Some people with accessory pathways do not have delta waves at baseline, some have them only sometimes, some delta waves are so intermittent that the same ECG will have some beats with delta waves and some without.  

Example: What do you think of this "Ventricular Bigeminy"?

  

The absence of delta waves is sometimes called "Concealed conduction", though this term has fallen out of favor.  See here about concealed conduction.

Wide Complex Tachycardia, and What is Latent Conduction and "Concealed Conduction?"

20-something with anxiety. Pulse is 169. Then 229. Then 169. Then 229. Latent conduction vs. Concealed Conduction. 3 Pathways.

Was it a good idea to try adenosine?

Yes.  A regular wide complex tachycardia in a young patient with no history of heart disease is very likely to be AVRT.   VT is not harmed by adenosine,

When is adenosine dangerous?

It is dangerous in WPW with atrial fibrillation.  It is NOT dangerous when the tachycardia is regular.  In Atrial Fibrillation, the tachycardia will always be irregularly irregular.  In Atrial fib with WPW, there will be polymorphic QRS complexes (in this case, all QRS complexes are identical).  There would also be some R-R intervals that are VERY short (less than 240 ms).

Case Continued

He underwent an MRI to look for scar as a nidus for VT:

IMPRESSION
1) Borderline LV function with no focal wall motion abnormalities
2) Normal dimensions of all cardiac chambers
3) No evidence of myocardial scar on delayed enhancement sequences after contrast administration
4) No MRI evidence of arrhythmogenic right ventricular dysplasia.

EP note:

"He had wide-complex monomorphic tachycardia with extreme axis concerning for VT. He is young and the tachycardia was not polymorphic in nature, so this is very unlikely to be an ischemic rhythm and much more likely scar mediated. He got an MR, however that showed no scar or evidence of AVRD and he had a stress test with no evidence of inducible ischemia with almost 20 METs." 

 

He underwent an EP study 5/10/2022 for evaluation of pre-excitation/accessory tract which found a left sided accessory pathway - he is currently in the EP study now. Cardiology consults will continue to follow in the morning and address necessary cardiology follow-up. 

 

EP study confirmed an accessory pathway.  It was ablated.

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MY Comment, by KEN GRAUER, MD (6/28/2023):

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There is a tendency for clinicians to interpret cardiac arrhythmias in binary fashion. By this I mean — that a given rhythm is interpreted as being either Diagnosis #1 or Diagnosis #2, with "nothing" in between. Clinically — this most often this relates to a rhythm being interpreted as either VT or SVT.

• In my opinion — it is a mistake to interpret arrhythmias in strict "binary" fashion — since rather than "either/or" — optimal interpretation is more of a probability statement.

To illustrate this concept — I've reproduced in Figure-1, the initial ECG recorded on today's patient in the ED.

• Rather than calling this rhythm "definitely" VT — optimal interpretation would entail description of this rhythm as a regular WCT ( = Wide-Complex Tachycardia) at ~225-230/minute, without clear sign of atrial activity.  

KEY Point: The principal differential diagnosis of a regular WCT rhythm without clear sign of atrial activity includes: i) VT (which statistically in an unselected adult population makes up at least 80% of cases); ii) Some type of SVT with either preexisting BBB or aberrant conduction; — or — iii) Something else (with this "something else" including entities such as hyperkalemia and/or WPW-related tachyarrhythmias).

• The above statistics are derived from an unselected adult population. Additional factors may help greatly to narrow down and increase relative probability of one or another diagnosis.
• For example — in an adult of a "certain age" (ie, a patient beyond the "young adult" age range — usually beginning near "middle-age") — IF the patient has underlying heart disease — then even before looking at the actual ECG, statistical odds that a regular WCT rhythm without sign of atrial activity will turn out to be VT approach 90%.
• Use of QRS morphology may help to further increase the accuracy of this prediction. For example, IF this patient were an adult of a "certain age" who had known underlying heart disease — the fact that the QRS complex during the WCT rhythm in Figure-1 is extremely wide — with an amorphous QRS complex in all anterior leads, in which there is very slow initial depolarization — with predominant negativity of the QRS in lead V6 — and — with a QRS morphology that fails to resemble any form of known conduction defect — would suggest >95-98% likelihood that this WCT rhythm was VT.

The above said — today's patient was not an older adult with known heart disease. Instead — today's patient was a previously healthy man in his 30s.

• Not commonly appreciated is how surprisingly common VT may be in younger adult patients who present with a regular WCT rhythm without clear sign of P waves. That said — such patients almost always have idiopathic VT, in which there is no underlying heart disease!
• I've reproduced in Figure-2 — the KEY features of QRS morphology characteristic of some form of idiopathic VT. These generally entail fascicular VT (most commonly manifesting RBBB-LAHB or RBBB-LPHB-like morphology) or RVOT VT (recognized by LBBB-like morphology in the chest leads with an inferior frontal plane axis). The marked QRS widening, with amorphous shape in anterior leads seen in today's tracing is clearly not suggestive of idiopathic VT. 
• 
  
• BOTTOM Line: As per Dr. Smith — the fact that today's patient was a previously healthy young adult who presents with the markedly abnormal QRS morphology seen in the WCT shown in Figure-1 — dramatically reduces the likelihood of VT (especially given no sign of anatomic cardiomyopathy on bedside ultrasound!).

Figure-1: The initial ECG that was recorded in the ED.

Final PEARL:

Although the differential diagnosis of an SVT with a wide QRS includes sinus tachycardia (with either preexisting BBB or aberrant conduction) and AFlutter — the rate of ECG #2 in Figure-1 ( = ~225-230/minute) — is too fast for sinus tachycardia in an adult — and "off" for either 1:1 or 2:1 AFlutter (in which the atrial rate of untreated flutter is typically between 250-350/minute).

• As per Dr. Smith — this establishes AVRT as the principal diagnostic consideration. The overwhelming majority of AVRT reentry SVTs are conducted "orthodromic" (ie, passing first down the normal AV nodal pathway — thereby resulting in a narrow QRS complex).
• That said — from 1-to-5% of reentry AVRT rhythms are "antidromic", in which the reentry circuit passes first down the AP (Accessory Pathway) — which results in a wide QRS. Antidromic AVRT is precisely the mechanism for the overly wide and unusual QRS morphology seen in today's case!
• There is a tendency to assume that regular WCT rhythms without atrial activity are VT. While true in >95% of cases — it is well to keep in mind that on occasion (especially in a previously healthy younger adult) — we may see a regular WCT due to antidromic AVRT. Distinctinction between antidromic AVRT and VT may not be possible from the single ECG obtained during the WCT rhythm (as was the case today!).

Figure-2: Review of the KEY features regarding Idiopathic VT (which I previously published in My Comment at the bottom of the page in the May 14, 2022 post in Dr. Smith's ECG Blog).